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There have been a number of exciting advances in the clinical management of concussion over the past several years. This article reviews new developments in concussion diagnosis technologies.
Recent research suggests that traditional biomechanical models of postural stability do not fully characterise the nonlinear properties of postural control. In sports medicine, this limitation is manifest in the postural steadiness assessment approach, which may not be sufficient for detecting the presence of subtle physiological change after injury. The limitation is especially relevant given that return-to-play decisions are being made based on assessment results. This update first reviews the theoretical foundation and limitations of the traditional postural stability paradigm. It then offers, using the clinical example of athletes recovering from cerebral concussion, an alternative theoretical proposition for measuring changes in postural control by applying a nonlinear dynamic measure known as 'approximate entropy'. Approximate entropy shows promise as a valuable means of detecting previously unrecognised, subtle physiological changes after concussion. It is recommended as an important supplemental assessment tool for determining an athlete's readiness to resume competitive activity.
The need for a measure of severity of concussion apart from duration of post-traumatic amnesia is examined. The paced auditory serial-addition test, a measure of rate of information processing, is presented as a convenient test for estimating individual performance during recovery. Procedures for administration and control data are given, and the programme used for managing the rehabilitation of concussion patients described.
This study is the first attempt to characterize neurological and behavioural consequences of fluid-percussion concussive head injury in the cat. Both animals initially anaesthetized by N2O as well as unanaesthetized, chronically prepared animals were subjected to injury. Injury with a fluid-pressure wave of 1.9-2.5 atm (duration 21-24 ms) produced a brief generalized areflexia. Following this initial response, injury greater than 2.1 atm frequently produced a period associated with hypotonia of postural muscles and suppression of postural motor responses (flaccidity). A close association between flaccidity and other indices of coma such as absence of eye-opening responses was noted. These consequences of injury can occur without fatal apnoae, circulatory collapse or overt intraparenchymal haemorrhages. This result suggests that mechanical stress predominantly restricted to the brain stem in fluid percussion may be sufficient, at least in the cat, to produce coma associated with flaccidity which has been previously documented for acceleration concussion. There was no evidence that fluid percussion produced EEG depression similar to the effects of lesions in the mesencephalic reticular activating system (RAS). Thus, depression of general levels of brain activity including those within the RAS seems not be necessary for production of this form of reversible coma.
Cerebral concussion was produced in rats by an iron pendulum hitting the external occipital protuberance. This resulted in loss of consciousness lasting from 3 to 10 minutes with prompt recovery and no focal neurological signs. The energy absorbed by the head at the impact was calculated to be about 1450 gm/cm. Light microscopic survey showed only minor pathological changes. However, electron microscopic observation revealed considerable alteration which began at 30 minutes, reached a peak at 1 hour, and disappeared at 24 hours after concussion. The salient changes included severe swelling of the neuronal mitochondria at the point of impact (occipital cortex), and extracellular edema at the site of contre coup (frontal lobe). Topographically, the most severe alteration was seen in structures at the craniospinal junction (medulla oblongata and upper cervical cord), consisting of both mitochondrial and edematous changes. Although there was no visible opening of the capillary interendothelial junctions, extravasated ferritin particles were accumulated in the edematous regions, indicating a transient increase in the permeability of the blood-brain barrier.
A leukotriene-like immunoreactivity was measured by radioimmunoassay in the gerbil forebrain following ischemia and reperfusion, subarachnoid hemorrhage (SAH), or nonlethal concussive brain injury. In each paradigm an increase in immunoreactivity levels was found. Peak levels were reached 15 to 30 minutes after each insult, and slowly returned to baseline over the next 24 hours. The study supports the suggestion that cerebral vessels and circulating blood are capable of producing leukotrienes, and that a major source of production is a nonvascular component within gray matter, possibly the cortical neuron. Leukotrienes may play a role in the pathophysiology of cerebral edema formation, cerebral vasospasm, seizure activity, and other central nervous system abnormalities. These studies are the first to demonstrate leukotriene production in gerbil brain following SAH or concussive brain injury.
This study examines the effects of concussive levels of a fluid-percussion head injury on sensory transmission within the lumbar spinal cord of the cat. Primary afferent depolarization (PAD) was suppressed for 2 to 5 minutes following injury, as assessed by dorsal root potentials and augmentation of antidromic dorsal root potentials, both evoked by stimulation of adjacent dorsal roots. Polysynaptic reflex discharges in ventral root potentials evoked by dorsal root stimulation were also profoundly suppressed during this same period, even when spontaneous and monosynaptic reflex discharges were facilitated. Changes in PAD produced by injury were abolished by spinal cord transection, but were not affected by midpontine transection. These findings suggest that concussive head injury can produce suppression of segmental sensory transmission by neurally mediated processes involving the bulbar brain stem. Recordings of dorsal root resting potentials, antidromic dorsal root potentials, and reductions of antidromic dorsal root potentials induced by tetanic root stimulation indicated that depressed segmental sensory function produced by injury was due to suppression of postsynaptic interneuronal transmission rather than to excitability changes in primary afferent fibers. Somatosensory cortical potentials evoked by dorsal root stimulation were profoundly depressed at the same time as segmental sensory transmission was suppressed, suggesting that suppressed segmental sensory transmission may also contribute to suppression of ascending sensory transmission. It is hypothesized that transmission failure of interneuronal systems in the initial period following insult may be a general response occurring in wide areas of the central nervous system, and not restricted to areas to which mechanical stress is directly applied. This response pattern may result from indiscriminate activation of interconnected excitatory and inhibitory elements of interneuronal systems.
An increase in extracellular K+ concentration ([K+]c) of the rat hippocampus following fluid-percussion concussive brain injury was demonstrated with microdialysis. The role of neuronal discharge was examined with in situ administration of 0.1 mM tetrodotoxin, a potent depressant of neuronal discharges, and of 0.5 to 20 mM cobalt, a blocker of Ca++ channels. While a small short-lasting [K+]c increase (1.40- to 2.15-fold) was observed after a mild insult, a more pronounced longer-lasting increase (4.28- to 5.90-fold) was induced without overt morphological damage as the severity of injury rose above a certain threshold (unconscious for 200 to 250 seconds). The small short-lasting increase was reduced with prior administration of tetrodotoxin but not with cobalt, indicating that neuronal discharges are the source of this increase. In contrast, the larger longer-lasting increase was resistant to tetrodotoxin and partially dependent on Ca++, suggesting that neurotransmitter release is involved. In order to test the hypothesis that the release of the excitatory amino acid neurotransmitter glutamate mediates this increase in [K+]c, the extracellular concentration of glutamate ([Glu]c) was measured along with [K+]c. The results indicate that a relatively specific increase in [Glu]c (as compared with other amino acids) was induced concomitantly with the increase in [K+]c. Furthermore, the in situ administration of 1 to 25 mM kynurenic acid, an excitatory amino acid antagonist, effectively attenuated the increase in [K+]c. A dose-response curve suggested that a maximum effect of kynurenic acid is obtained at a concentration that substantially blocks all receptor subtypes of excitatory amino acids. These data suggest that concussive brain injury causes a massive K+ flux which is likely to be related to an indiscriminate release of excitatory amino acids occurring immediately after brain injury.
80 children of preschool age were observed after concussion of the brain. In follow-up from 6 months 3 years clinical-anamnestic and neuropsychologic methods were used. The functions of autonomic nervous system were evaluated according to the results of estimation of initial autonomic tonus, autonomic reactivity, autonomic maintenance of the activity and the data of cardiointervalography. The state of nonspecific systems of the brain was studied with day time polygraphic research with a visual EEG evaluation, construction of histogramms by Fora method, estimation of speed and order of the fading of the components of a rough response. Psychovegetative stress was the ground for neurologic disorders in posttraumatic period. The disorders of adaptive regulation were manifested in exhausting of ergotropic systems with compensatory overstrain of trophotropic mechanisms, resulted in predominance of inhibiting influences with an inadequate response of synchronization on EEG during functional loads. Severity of clinical manifestations and disorders of adaptive regulation were more pronounced in children 1-3 year-old and with hypoxic-traumatic damages of the brain in anamnesis. Disintegration of cerebral activity correlated with the remote period. In the first 6-12 months after the concussion of the brain changes of vegetative reactivity prevailed, after 18 months the alterations in vegetative maintenance progressed.
The aim of the study was to study the count of circulating immune complexes (CIC) in the blood of children with acute concussion of the brain. The fact that CIC at high concentrations that can penetrate into the brain through the blood-brain barrier and cause complications as vasculitis, microangiopathy, proliferative processes in the meninges, enlarged ventricles of the brain, and atrophy of its tissue was borne in mind. The studies revealed a significant progressive CIC increase within 3 weeks. For correction of blood CIC levels, laser exposure was applied to the carotid and vertebral arteries and acupuncture points. For comparison, thymaline in age-specific doses was used. Laser radiation showed a significant fall of CIC at days 19-21, particular when applied to the acupuncture points. Thymaline did not affect blood CIC levels. Laser application to the acupuncture points in children with acute brain concussion should reduce the incidence of complications of brain injury disease.
As many as 140 patients aged 16 to 75 years with a history of brain concussion were under observation. The observation periods were from 1 to 2 months after the acute period elapse up to 25 years. In addition to neurological examinations, the patients were subjected to echoencephalography, computer-aided tomography of the brain (38 patients), ultrasound tomoscopy of the brain (40 patients and 30 healthy subjects). It has been shown that the use of echoencephalography, computer-aided tomography and ultrasound tomoscopy of the brain makes it possible to identify, in some cases, different disorders on the part of the brain. The role of these methods in the diagnosis of brain concussion consequences increases, provided they are used combined or jointly with the data obtained during clinical examination and observation.
Content of fatty acids in rabbit brain hemispheres in dynamics of experimental brain concussion was estimated by means of gas liquid chromatography. Content of fatty acids was increased within 15 min after experimental brain concussion and then it decreased reaching minimal values within 7 days. The phenomenon observed is a pathogenetically important factor in the traumatic disease.
The material contains 128 cases of brain concussion diagnosed by physicians since 1995 to 2000. The bases of diagnosing and the rules of opinionating of brain concussion after trauma of the head were discussed. Inconsistencies between clinical diagnosis and forensic medical opinionating were observed in 69.53%. In the group of patients who were intoxicated at the moment of head trauma disagreement was observed in 91.30%.
Athletes sustaining a concussion should be held from contact activities a minimum of 7 days; they must be asymptomatic and their coordination and neuropsychological tests should have returned to their pre-injury baseline (strength of recommendation [SOR]: B, based on multiple prospective cohort studies). High-risk athletes (eg, those with a history of previous concussion, high-school age or younger, or female) may need to avoid contact even after all these criteria are met (SOR: C, expert opinion).
There is an epidemic in our midst that most of us are unaware of. Untold numbers of young people are suffering concussions at an alarming rate. Many go unreported. The public as well as the medical profession have failed to appreciate the consequences of this problem and have been unaware of its significance and its long-term complications. In order to prevent both the short and potentially long-term functional brain impairment that may occur if a concussion is not treated properly, the following management recommendations are outlined.
Acoustic truncal evoked potentials (ATEP) were studied in 24 patients in the first 48 hours after concussion of the brain. The absolute peak latency of components 1, 3, and 5, the interpeak intervals 1-3, 3-5, and 1-5, and the interaural difference were determined. The results were compared with those of examination of a control group of 24 healthy individuals. Individual and group appraisal failed to reveal any significant differences from normal values in none of the studied parameters in patients with brain concussion. The informativeness of the method in mild craniocerebral trauma is discussed.
The author presents data on 168 patients: 75 during the acute period of brain concussion and 93 in the remote period of brain concussion. Age of the patients from 15 to 75 years. Drug treatment in these patients was combined with psychotherapy. Data are reported on the methods of psychotherapy including patients that suffered of concomitant chronic neurological and somatic diseases.
A stystematic neurological and electroencephalographical follow-up study in 344 head injured adults gave the following results: 1. 52% of all the hospitalized (mostly primarily amnesic) patients had a cerebral contusion. A contusion was assumed in cases with focal neurological signs (13%), amnesias of more than 8 hours (16%) and/or EEG-abnormalities lasting for more than 24 hours (49%). 2. Traumatic EEG-abnormalities were general slowing (43%) and foci (32%). In 40% of the cases with general slowing the slowing (greater than or equal to 1.5/sec) was within the alpha-frequency band and could only retrospectively be assed. 3. The EEG was invariably abnormal in cases with an amnesia exceeding 8 hours. If the amnesia exceeded 1 hour abnormalities were found in 73%. 4. Among the patients with contusion 6.5% had no amnesia, 48% less than 30 minutes and only 30% an amnesia for more than 8 hours. In 75% of the patients with concussion amnesia lasted less than one hour. 5. Skull fractures were mostly combined with contusion (74%). 6. Impaired drive, reduced ability to concentrate, memory deficits, headache and dizziness were significantly more frequent 6 months after contusion than after concussion. 7. 21% of the patients with traumatic dizziness (44%) had a labyrinthine contusion. 8. Among the contusions diagnosed with the aid of EEG recordings 58% would have been missed after exclusive neurological examination and 82% after application of the classical criteria used by surgeons and general practitioners.